ArticleCell death discovery2024
The combination of temozolomide and perifosine synergistically inhibit glioblastoma by impeding DNA repair and inducing apoptosis.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Bibliometric and visualization analysis of glioma pharmacotherapy from 2020 to 2024.Frontiers in neurology · 2025Pooled it
- RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.Science advances · 2026Article
- Al- and Ga-doped graphitic carbon nitride as a temozolomide nanocarrier platform: a DFT study of adsorption and interfacial interactions.Nanoscale advances · 2026Article
- Reprogramming temozolomide response in glioblastoma through regulated and immunogenic cell death modalities.Cell death discovery · 2026Review
- Disrupting Akt-Wnt/β-catenin signaling suppresses glioblastoma stem cell growth and tumor progression in immunocompetent mice.Journal of neuro-oncology · 2026Article
- Combination Cancer Therapy and Reference Models for Assessing Drug Synergy in Glioblastoma.Current oncology (Toronto, Ont.) · 2025Review
- Review
- AMPA Receptor Modulation in the Treatment of High-Grade Glioma: Translating Good Science into Better Outcomes.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Tinostamustine (EDO-S101) and Its Combination with Celecoxib or Temozolomide as a Therapeutic Option for Adult-Type Diffuse Gliomas.International journal of molecular sciences · 2025Article
- Mouse pancreatic tumor organoids reveal synergistic efficacy of low-dose anticancer drug and radiation combinations.Frontiers in medicine · 2025Article
- Tight junction proteins in glial tumors development and progression.Frontiers in cellular neuroscience · 2025Review
- Identification and validation of TSPAN13 as a novel temozolomide resistance-related gene prognostic biomarker in glioblastoma.PloS one · 2025Article
- Role of BRCA1 in glioblastoma etiology.Cellular oncology (Dordrecht, Netherlands) · 2024Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Temozolomide (TMZ) is widely utilized as the primary chemotherapeutic intervention for glioblastoma. However, the clinical use of TMZ is limited by its various side effects and resistance to chemotherapy. The present study revealed the synergistic inhibition of glioblastoma through the combined administration of TMZ and perifosine. This combination therapy markedly diminished BRCA1 expression, resulting in the suppression of DNA repair mechanisms. Furthermore, the combination of TMZ and perifosine elicited caspase-dependent apoptosis, decreasing glioblastoma cell viability and proliferation. The observed synergistic effect of this combination therapy on glioblastoma was validated in vivo, as evidenced by the substantial reduction in glioblastoma xenograft growth following combined treatment with TMZ and perifosine. In recurrent glioma patients, higher BRCA1 expression is associated with worse prognosis, especially the ones that received TMZ-treated. These findings underscore the potent antitumor activity of the AKT inhibitor perifosine when combined with TMZ and suggest that this approach is a promising strategy for clinical glioblastoma treatment.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.